Gastric cancer has been and remains the second most common cause of cancer death and the third most common cancer worldwide [1]. Recently, gastric cancer therapy has received more attention, since neoadjuvant modalities have shown to improve outcome for respectable tumors [2-4]. In this respect, molecular surrogate marker(s) of disease outcome could be of benefit in the management of gastric cancer patient treatment. Furthermore, because gastric cancer is relatively resistant to chemotherapeutic agents, prognostic molecular determinants in gastric cancer could help improve adjuvant regimens.
About 60% of human genes are associated with clusters of CpG dinucleotides, referred to as CpG islands [5]. Clustered methylation of CpG islands at a gene promoter or transcription start site is associated with gene silencing. This epigenetic event has been observed in many genes of different cancers [6]. Hypermethylation of tumor-related regulatory genes may play a significant role in tumor transformation and progression, impacting the clinical course of disease. Several recent studies have focused on hypermethylation of specific tumor-related genes which appears to suppress growth and proliferation of gastric cancer [7-11]. Genes regulated by methylation status can significantly alter tumor suppressor functions as well as tumor-inducing capacities. Therefore, gene inactivation by hypermethylation may have dual effects on tumorigenesis and tumor progression.
To date, epigenetic inactivation of genes related with tumor progression has not been well studied in gastric cancer as related to disease outcome.